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N361: Pathophysiology II > Module 2 - Alterations in Fluids and Electrolytes > Flashcards

Module 2 - Alterations in Fluids and Electrolytes Flashcards

1
Q

Every disease process involves some alteration in ..

A

fluids and electrolytes

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2
Q

Molecule

A

When two or more atoms combine to form a substance

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3
Q

Ion

A

an atom carries an electrical charge because it has either gained or lost electrons

some ions have a negative charge and some positive charge

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4
Q

Cation

A

Ion that carries a positive charge and it has given away or lost electrons

Positive charge

fewer electrons than protons

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5
Q

Anion

A

an ion that has gained electrons and therefore carries a negative charge

negative charge

gained or taken on electrons (more electrons than protons)

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6
Q

In health there is ___ amounts of cations and anions in the body

A

equal

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7
Q

Electrolytes

A

substance dissolved in solution and some of its molecules split or dissociate into electrically charged atoms or ions

critical for life and muscle function

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8
Q

What is the unit of measurement for volume of fluids ?

A

metric - L or mL

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9
Q

In the body, non-dry areas are in ___

A

solution

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10
Q

The unit of measure that expresses the combining activity of an electrolyte is …

A

the milliequivalent (mEq)

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11
Q

One mEq of any cation will …

A

always react chemically with one mEq of an anion

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12
Q

What information does mEq’s provide?

A

information about the number of cations or anions available to combine with other cations or anions

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13
Q

The fluid in each of the body compartments contains …

A

a particular composition of electrolytes which differ from that of other compartments

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14
Q

To function normally, body cells must have …

A

the right amount of fluids and electrolytes (and being in the right compartments)

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15
Q

Whenever an electrolytes moves out of a cell..

A

another electrolyte moves in to take its place

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16
Q

Homeostasis

A

a state that requires the number of cations and anions to be the same in order to exist

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17
Q

Body compartments are separated by..

A

semi permeable membranes

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18
Q

Intracellular Compartments

A

Fluids inside the cells

Most of the body fluid (2/3) is inside the cells

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19
Q

Extracellular Compartments

A

Refers to all fluid outside the cells (plasma, blood, interstitial fluids)

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20
Q

Intravascular Compartment

A

Fluids in the blood vessels (ECF subtype)

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21
Q

Interstitial Fluids

A

fluid between the cells and blood vessels

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22
Q

What compartment is the most important to view electrolyte levels from?

A

The intracellular compartments (ex: potassium is highest in the cell, not blood or ECF; almost no calcium in cells; small traces of Na, etc)

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23
Q

Most sodium is in …

A

the blood

(this is also the most sensitive electrolyte to the blood)

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24
Q

What does body fluid do for us?

A

Transports nutrients to the cells and carried waste products from the cells

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25
Q

How much of the body weight is body fluids?

A

60%

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26
Q

What losses of body fluid are serious or fatal?

A

Serious - 10%
Fatal 20%

ex: 70 kg person has about (152 lbs) 42 L of body fluids (60%). 4.2 L 10%, and 20% is 8.4 L

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27
Q

How might body fluid amounts be different?

A

Older people usually have less fluid; Muscular people often have more

So factors other than just loss is important like age and situation

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28
Q

Body fluid consists of what?

A

Water and dissolved substances

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29
Q

The largest single fluid constituent of the body is ..

A

water

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30
Q

Why is it important whether a substance dissolves or not in solution?

A

Some do not dissolve, glucose, urea, and creatinine, and therefore cannot be moved as simple substances

Some larger ones do (ex: NaCl) and then their constituents can be moved easily

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31
Q

What is the ratio of ECF to ICF in the body

A

2/3 ICF to 1/3 ECF

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32
Q

Of extracellular fluid, what makes it up?

A

80% Interstitial Fluid

20% Plasma

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33
Q

How does body fluid differ between genders?

A

Males are 40% solid and 60% fluid, and Females are 45% solid and 55% fluids

Women naturally have more body fat so they have less fluid, and fat does not hold water like muscle does

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34
Q

How does body fluid correlate to muscle and fat?

A

Increased fat = decreased total body water

Increased muscles = increased total body water

So, even if a person is heavier, they are at risk for dehydration

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35
Q

Diffusion

A

the movement of particles in all directions through a solution

the process by which a solute may spread through a solution or solvent

Goes from high to low concentration with little/no energy used

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36
Q

Solute

A

the substance that is dissolved

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37
Q

Solvent

A

the solution in which the solute is dissolved

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38
Q

When a solute diffuses how does it spread the molecules?

A

It spreads the molecules from an area of high concentration to an area of lower concentration (not a lot of energy to do this)

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39
Q

Permeable Membrane

A

a membrane allowing substances to pass through/diffuse without restriction

we do not want these, we want some control

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40
Q

Selectively Permeable Membrane

A

membrane allowing some solutes to pass through without restriction but will prevent others from passing freely

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41
Q

Osmosis

A

Like a PULL of water or solvent across a membrane

occurs when there is a more concentrated solution on one side of a selectively permeable membrane and a less concentrated solution on the other side - so osmotic pressure draws water through the membrane to the more concentrated side or the side with more solute

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42
Q

Water Osmosis occurs from ___ concentrated to ___ concentrated

A

low concentration to more concentration (in order to have equal concentrations on each side)

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43
Q

Osmotic Pressure

A

force that draws the water (pull) from less concentrated solution through a selectively permeable membrane into a more concentrated solution

the difference determines strength

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44
Q

Hydrostatic Pressure

A

the force for filtration (PUSH pressure) - like water pushing against a water balloon

the force exerted by the weight of a solution

it moves from an area of greater pressure to an area of lesser pressure

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45
Q

Filtration

A

movement of solutes and solvents by hydrostatic pressure

it moves from an area of greater pressure to an area of lesser pressure

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46
Q

Osmolality

A

refers to the number of osmotically active particles per kilogram of water

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47
Q

What unit is osmotic pressure measured in

A

Milliosmols

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48
Q

Normal osmolality of plasma is …

A

280-294 mOsm/kg

just a little less than 300

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49
Q

When there is a difference in hydrostatic pressure on two sides of a membrane, ___ and ___ ____ move out of the solution that has the ___ hydrostatic pressure by process of ____

A

When there is a difference in hydrostatic pressure on two sides of a membrane, water and diffusible solutes move out of solution that has the higher hydrostatic pressure by process of filtration

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50
Q

How does pressure differ at the arterial end of the capillary?

A

At the arterial end, hydrostatic pressure or push is greater than osmotic pressure - so more fluids and diffusible solutes move out of the capillary (via filtration)

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51
Q

How does pressure differ at the venous end of the capillary?

A

At the venous end, osmotic pressure or pull is greater than hydrostatic pressure - so fluids and some solutes move into the capillary (via osmosis)

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52
Q

What occurs to excess fluid and solutes remaining in interstitial spaces after osmosis and diffusion?

A

The excess fluid and solutes are returned to intravascular compartment by lymph channels

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53
Q

What separates interstitial fluid from intravascular fluid?

A

cell membranes (selectively permeable - may need energy like ATP with the NaK Pump)

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54
Q

The greater the number of particles in a concentrated fluid, the more ___ there will be to move ___ through the memvbrane

A

pull; water

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55
Q

Isotonic Solution

A

“Same”

Solutions on both sides of the membrane have established equilibrium or are equal in concentration

Equal tonicity - no shift in fluid

Isotonic solutions have the same tonicity as body fluids

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56
Q

Tonicity

A

refers to concentration of dissolved molecules held in solutions

isotonic solutions have same tonicity as body fluids and it occurs between the membranes

this refers to being hypotonic, isotonic, and hypertonic

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57
Q

Examples of Isotonic Solutions

A

0.9% Sodium Chloride(Isotonic Saline / Normal Saline) - good for replacing fluid volumes

5% Dextrose

5% Dextrose in 0.225% Saline

Lactated Ringer’s Solution (for emergencies)

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58
Q

There is ___ to ___ mOs/kg in Normal Saline

A

280 to 294

(same osmolality as plasma)

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59
Q

What occurs for movement when an isotonic fluid is given?

A

little fluid movement / osmosis occurs

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60
Q

Hypotonic Solutions

A

When a solution has a lower concentration of salt than other solutions - it is hypotonic

It has less salt OR more water than isotonic

Fluid ends up moving into the cells

Restores cells from dehydration

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61
Q

Examples of Hypotonic Solutions

A

0.45% Saline (dilutes blood by moving fluid into the cells - moves from a less concentrated to more concentrated)

Distilled Water (no solutes)

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62
Q

What is the highest electrolyte in the blood

A

Salt

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63
Q

Hypertonic Solutions

A

A solution that has a higher concentration of solutes than another solution is a hypertonic solution

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64
Q

Examples of Hypertonic Solutions

A

10% dextrose in water

5% dextrose in 0.9% saline

5% dextrose in 0.45% saline

5% dextrose in lactated Ringer’s Solution

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65
Q

What is the difference in hypotonic and hypertonic concentrations for blood and cells?

A

Hypotonic - fewer particles in blood, but more in the cell, so the cell gets water moving in and causes swelling (a problem)

Hypertonic - more particles in the blood and fewer in the cells, so water moves out of cells to the blood - this dehydrates the cells

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66
Q

If the selectively permeable membrane will allow the solvent to pass through but will not allow the solute through freely…

A

the solvent will move to the side of greater solute concentration

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67
Q

If the extracellular fluid is 300 mOsm/kg in 17 L and inside the cell is 280 mOsm/kg in 25 L, what is the tonicity and changes after osmosis?

A

The ECF is hyperosmotic with ICF being Isotonic

It will go from 300 in 17L in the ECF to 290 in 18 L; It will go from 280 in 25 L in the ICF to 290 in 24 L - this occurs because the water moves from inside the cell moves out to the higher concentration

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68
Q

If the ECF is 260 mOsm/kg in 19 L and ICF is 280 mOsm/kg in 25 L, what is the tonicity and changes after osmosis?

A

ECF is hypotonic with the inside of the cell being isotonic

ECF goes 260 in 19 to 270 in 18 while ICF goes 280 in 25 to 270 in 26

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69
Q

Hypertonic solutions cause ___ while Hypotonic solutions cause ___

A

shrinkage ; swelling

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70
Q

Active Transport

A

moving an ion from low concentration to high concentration requires energy and active transport

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71
Q

Active transport moves molecules or ions ___ concentration and osmotic pressure

A

against

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72
Q

Energy for active transport is supplies by ___ ___ in the cell

A

metabolic processes (ex: ATP)

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73
Q

What are some substances that require active transport to move through the cell membranes

A

Na Ions, K ions, Ca, Iron, Hydrogen, some sugars, amino acids

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74
Q

What ways do fluids leave the body

A

Skin
Lungs
GI Tract
Kidneys

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75
Q

The ___ excrete the largest quantity of fluid

A

kidneys

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76
Q

__ of urine can tell a lot about extra fluid amounts in the body

A

color

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77
Q

How much water is lost by the skin via diffusion per day?

A

300-400 mL per day

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78
Q

Water loss from perspiration depends on what?

A

depends on the temperature of the environment and of the body

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79
Q

Average amount of water lost via perspiration is ___ mL per day

A

100

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80
Q

How is water lost by the lungs and how can the amounts change?

A

lost via expired air which is saturated with water vapor

amount varies with the rate and depth of respiration

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81
Q

Average amount of water lost from the lungs is …

A

300-400 mL per day

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82
Q

Insensible Loss

A

water lost from lungs and skin that is lost without the person being aware of the loss

You are unaware and cannot be measured

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83
Q

How does body fluid excretion relate to the GI tract

A

very large amounts of electrolyte containing liquids are secreted into the GI tract but almost all of this fluid is reabsorbed - and returns again to the ECF

A LOT of it is reabsorbed

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84
Q

The average amount of water lost in the feces is ___ mL/day which is equal to ….

A

200 mL/day which is equal to the amount of water gained through oxidation of foods

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85
Q

How does severe diarrhea influence electrolyte and fluid balance?

A

loss of large quantities of fluids and electrolytes occurs

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86
Q

What organ plays a major role in regulating fluid and electrolyte balance?

A

Kidneys - they can adjust the amount of water and electrolytes leaving the body

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87
Q

What determines the quantity of fluid excreted by the kidneys?

A

determined by the amount of water ingested and the amount of waste and solutes excreted

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88
Q

Usual quantity of urine output is approximately ____; but this can vary greatly depending on ….

A

1500 mL per day

Fluid Intake
Amount of Perspiration
Other Factors

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89
Q

Daily Body Fluid Excretion?
Skin by Diffusion = __
Skin by Perspiration = __
Lungs = __
Feces = __
Kidneys = __
Total = __

A

Diffusion (Skin) - 350 mL
Perspiration (Skin) - 100 mL
Lungs - 350 mL
Feces - 100 mL
Kidneys - 1500 mL
Total - 2400 mL / day

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90
Q

What are the three sources for water entering the body?

A

Oral Liquids

Water in Foods

Water formed formed by oxidation of foods

(this includes tubes when doing I&O)

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91
Q

Average total amount of water taken into the body by the 3 sources of water is ___ mL per day

A

2400 mL/day

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92
Q

About how much water is released by metabolism of each 100 calories of fat, carbs, and proteins

A

10 mL

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93
Q

How are electrolytes replaced?

A

Electrolytes are present in foods and liquid and in a normal diet an excess of essential electrolytes is taken and the unused electrolytes are excreted via urine

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94
Q

Homeostasis

A

Balance

a term which indicates the relative stability of the internal environment

It is needed because concentration and composition of body fluids must be nearly constant

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95
Q

How is homeostasis directed in the deficiency and excess of electrolytes?

A

Deficiency - must replace fluids and electrolytes via either intake of food and water or by therapy like IV or meds

Excessive - excess fluid or electrolytes needs therapy or diuretics directed toward assisting the body to eliminate the excess

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96
Q

Kidney role in maintaining fluid and electrolyte balance

A

play a major role in controlling all types of balance in fluid and electrolytes

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97
Q

Adrenal Glands role in maintaining fluid and electrolyte balance

A

it secretes aldosterone (direct sodium -retention- which water follows)

it ends up aiding in controlling ECF volume by regulating the amount of sodium reabsorbed by the kidneys

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98
Q

ADH role in maintaining fluid and electrolyte balance

A

Antidiuretic hormone from pituitary gland regulates osmotic pressure of ECF by regulating amount of water reabsorbed by the kidneys

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99
Q

ADH and Aldosterone lead to ..

A

increased fluid volume (low flow states to the kidneys)

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100
Q

Factors that influence fluid intake

A

Climate

activity level (like breathing faster using more fluid)

social events

emotions (binge or anorexia)

LOC - confused/coma

age-elderly (decreased sense of thirst, loss of taste buds, immobility, purposeful restriction, confusion and depression)

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101
Q

What are the total gains and loss of fluid in a day?

A

Gain = liquids 1100-1400 + solid foods 800-1000 + oxidation of CHO, proteins, fats 200-350 = 2500 mL/day

Loss = respiration 300-400 + skin 300-400 + sweat 100 (1-2 L with exercise) + feces 100 + urine 1500 = 2500 mL/day

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102
Q

A lot of things are reabsorbed by the kidneys, but one thing that does not get reabsorbed is a good indicator of kidney function?

A

Creatinine (1.4 g)

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103
Q

_____ is a potent vasoconstrictor

A

Angiotensin II

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104
Q

What does aldosterone control?

A

salt which water then follows –> increased circulating volume

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105
Q

Pathway of the RAA system?

A

Renin release stimulated by low flow states to the kidneys and angiotensinogen works with it –> angiotensin I –> converted via enzyme to Angiotensin II –> Renal autoregulation, increased blood pressure, increased circulating volume

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106
Q

What gland releases Renin/RAA?

A

adrenal medulla

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107
Q

What gland releases ADH

A

posterior pituitary

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108
Q

What does ADH control?

A

governs water to increase fluid volume

does this by telling kidneys to hold water and decrease osmolarity of plasma until it is right and gets negative feedback

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109
Q

ADH pathway?

A

increased plasma osmolarity or decreased circulating blood volume –> thirst –> increased fluid intake –> increased water retention

increased plasma osmolarity or decreased circulating blood volume –> ADH secretion –> decreased water excretion –> increased water retention

Increased water retention –> increased circulating fluid volume -> decreased plasma osmolarity –> decreased ADH and thirst

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110
Q

What things does decreased blood volume, increased serum osmolarity, and increased thirst and water intake lead to? (RAA and ADH)

A

stimulates ADH production in hypothalamus

stimulate increased ADH release into the blood stream from posterior pituitary

decreased arterial BP

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111
Q

What does a drop in arterial blood pressure lead to? (RAA and ADH)

A

increased sympathetic discharge –> decreased renal perfusion –> increased renin release –> angiotensin I and II –> increased aldosterone by the adrenal cortex –> drop in salt and H2O excretion and an increase in blood pressure

increased sympathetic discharge –> decreased renal perfusion –> drop in water and salt filtered by the kidneys –> drop in salt and H2O excretion and an increase in blood pressure

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112
Q

What does a drop in salt and H2O secretion and an increase in blood pressure lead to? (RAA and ADH)

A

increased circulating volume of water and H2O with a loss of potassium –> increased blood volume and decreased serum osmolarity –> increased ADH production in hypothalamus

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113
Q

What does Increased ADH release into the blood stream from the posterior pituitary lead to? (RAA and ADH)

A

increased reabsorption of H2O by the kidneys –> decreased urine secretion –>increased circulating volume of water and H2O with a loss of potassium –> increased blood volume and decreased serum osmolarity –> increased ADH production in hypothalamus

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114
Q

The best way to measure daily fluid volume is …

A

Daily Weight

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115
Q

Why can I&O be inaccurate?

A

it can be hard to get every bit of intake and output

but it is a way to measure fluid weight / balance

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116
Q

Fluid Volume Deficit

A

dehydration in which water and electrolytes are lost in the same proportion

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117
Q

Goal of Fluid Volume Deficit treatment is to …

A

goal of treatment is to restore fluid volume, replace electrolytes as needed, and eliminate the cause of the fluid volume deficit

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118
Q

Causes of Fluid Volume Deficit

A

vomiting

diarrhea

increased respiration

use of diuretics and increased urine output

insufficient IV fluid replacement

GI suctioning

draining fistulas

ileostomy or colostomy drainage

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119
Q

How/things to/that assess fluid volume deficit?

A

increased respiration

increased heart rate

decreased central venous pressure (CVP)

weight loss

poor skin turgor

dry mucous membranes

decrease in urine volume

urine is dark in color and odorous

increased specific gravity of the urine

increased hematocrit

altered level of consciousness

confusion

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120
Q

Things to Implement for Fluid Volume Deficit

A

Assess vital signs

assess neck and hand vein turgor

assess mucous membranes and skin turgor

monitor hematocrit and electrolyte values

replace fluids by PO or IV (lactated ringers solution, 0.9% normal saline) as prescribed

administer medications as prescribed

monitor weight daily

monitor I&Os

test urine for specific gravity

monitor bowel sounds

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121
Q

Hypovolemia

A

Greater fluid loss than fluid intake

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122
Q

Isotonic Hypovolemia

A

this is Total Fluid Volume deficit

water and lytes (Na+) lost in equal proportions

ECF is iso-osmolar –> no change in ICF

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123
Q

Hypotonic Hypovolemia

A

decrease in solutes but not the water

so, ECF is hypo-osmolar –> fluid shifts from ECF to ICF (in cell causes swelling)

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124
Q

Hypertonic Hypovolemia

A

decrease in water but not solutes

ECF is hyper osmolar –> fluid shifts from ICF to ECF (shrinkage & dilute blood)

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125
Q

When talking about Hyper, Hypo, and Isotonic issues we are talking about …

A

the BLOOD

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126
Q

Etiologies of Hypovolemia

A

GI Fluid Loss
Kidneys
Hyperosmolar Tube Feedings
Fever
Decreased Fluid Intake
Skin
Hemorrhage
Third Spacing

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127
Q

What tonicity fluid hypovolemia does GI fluid loss get and examples of this loss?

A

Isotonic, Hypotonic

Prolonged vomiting
gastric suction
excessive diarrhea

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128
Q

What tonicity fluid hypovolemia does Kidney loss get and examples of this loss?

A

Isotonic, Hypotonic

Polyuria d/t DKA
Renal Disease
Diuresis

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129
Q

What tonicity fluid does hypovolemia due to fever loss get?

A

Hypertonic

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130
Q

What tonicity fluid does hypovolemia from decreased fluid intake get and examples of this loss?

A

Isotonic and Hypertonic

Decreased LOC, sedation, NPO status
Anorexia, N/V, Dysphagia
Decreased Access, Depression

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131
Q

Examples of hypovolemic fluid loss from skin?

A

Excessive sweating

burns

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132
Q

Why would we give isotonic and then hypotonic fluids to hypovolemics?

A

If there was loss from the GI or kidneys the isotonic can replace fluid volume and then the hypotonic solution moves fluid into the cells

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133
Q

Why would we give hypertonic solution to someone with a fever (hypovolemia)

A

Cells are getting more fluid than blood because of increased metabolic demand so this will bring fluid back into the blood

134
Q

Why would we give isotonic and then hypertonic fluids ?

A

if they have decreased fluid intake the isotonic will correct circulating volume and then the hypertonic fluids prevent cell and brain swelling

135
Q

Third Spacing

A

there is an appropriate amount of fluid in the body but it is stuck in the interstitial space between cells and the blood

this can lead to hypovolemia

136
Q

Why do we give isotonic fluids to third spacing?

A

it reestablishes circulating volume

137
Q

What are some manifestations of Hypovolemia?

A

Rapid weight loss (1 L = 1 kg = 2 lbs; 1 lbs = 500 mL)

Decreased skin turgor

oral changes (dry membranes; longitudinal furrows on tongue)

Decreased urinary output (oliguria <30 mL/hr or <400mL/24 hrs; increased urine specific gravity > 1.030)

increased BUN (>10:1 BUN:Creat ratio)

VS changes (decreased T, increased RR, orthostatic hypotension, increased FVD –> decreased BP in all positions)

Decreased CVP (JVD)

Decreased peripheral blood flow (>3 cap refill; cold extremities)

increased thirst, HCT, confusion, weakness

138
Q

BUN

A

nitrogen in the blood (urea)

increase BUN indicates decreased renal function or dehydration (increased ratio is concerning)

139
Q

How should solutions be taken in mild hypovolemia and severe hypovolemia?

A

Mild - Oral Intake
Severe - IV Fluids

140
Q

How should treatment go for Hypovolemia?

A
  1. Isotonic Solutions (NS or LR) to re-expand plasma volume, increase BP, and possibly administer blood if d/t hemorrhage
  2. Once normotensive, give a hypotonic solution (ex: 1/2 saline) to provide lytes and free water to make urine (ECF –> ICF)
141
Q

Fluid Challenge

A

Something we do if we are unsure if the hypovolemia is due to a kidney problem or volume problem

We give a bolus of water and if they do not increase urination then it may be a kidney problem, but good urinary output indicates dehydration.

142
Q

Nursing Interventions for Hypovolemia

A

Measure I and O

Daily Weight

VS

Skin

BUN:Creat Ratio

CVP

PO Intake - oral care (consider tube feedings if cannot PO)

Turn and Position - Moisturize Skin

Evaluation of Adequate Fluid Replacement

143
Q

What should be some signs of adequate fluid replacement from Hypovolemia?

A

increased urinary output (40-60 mL/hr)

decreased urine specific gravity

increased body weight

T, BP, HR, RR normal

skin turgor, oral moisture

increased CVP

increased sensorium and strength

144
Q

Fluid Volume Excess

A

actual excess of total body fluid or a relative fluid excess in one or more fluid compartments

also called Overhydration or Fluid Overload

Hypervolemia

145
Q

What is the goal of fluid volume excess treatment?

A

restore fluid balance, correct electrolyte balances, and eliminate or control the underlying cause of the overload

146
Q

Difference between Peripheral Edema and Cellular Edema?

A

Peripheral Edema is ECF fluid excess leading to fluid between the cells

Cellular Edema is ICF fluid excess leading to fluid in the cells

147
Q

Hypervolumia

A

Fluid intake > Fluid loss

148
Q

Isotonic Hypervolemia

A

water and lytes (Na+) gained in equal proportions

ECF is iso-osmolar –> no change in ICF

149
Q

Hypotonic Hypervolemia

A

Water intoxication

increase in water but not solutes

ECF is hypo-osmolar –> fluids shift ECF to ICF

150
Q

Hypertonic Hypervolemia

A

Increase in solutes but not water

ECF is hyper-osmolar –> fluid shifts ICF to ECF

151
Q

Etiologies of Hypervolemia

A

Excessive intake of sodium and water either PO or IV

Fluid retention d/t renal failure, SIADH (brain lesions can do this), cardiac disease (does not move water well), corticosteroid use (puffiness), cirrhosis of the liver, analgesic/anesthetic/psychotropic use

152
Q

The Major cause of Hypervolemia is …

A

Heart Disease

153
Q

Manifestations of Hypervolemia

A

Rapid Weight Gain (5-7 pounds is severe)

Circulatory Overload (Heart Failure)

Interstitial Edema (peripheral edema (dependent) when legs are down; pulmonary edema (inspiratory fine crackles = minimum of 1500 cc) which can be life threatening

JVD - distended neck veins

Bounding pulse

154
Q

Treatment for Hypervolemia

A

sodium restricted diet

diuretics

fluid restriction

155
Q

Why would a sodium restricted diet be used for Hypervolemia?

A

if the hypervolemia is d/t HF, RF, liver disease, HTN (cautiously)

156
Q

Loop Diuretic

A

lasix, bumex

works on the loop of henle

stronger diuretic

157
Q

Thiazide Diuretic

A

HCTZ (not for HF or RF)

not as strong as loop so its not for HF or RF

158
Q

K Sparing Diuretic

A

Aldactone

not as strong as loop or thiazide so not for HF or RF use either

159
Q

Can diuretics fix everything for Hypervolemia?

A

no

it could even reverse the problem to hypovolemia

160
Q

What things can Diuretics cause?

A

FVD

Hyponatremia

Potassium Imbalances

Loss of Mg

Changes in Ca Excretion

Acid Base Problems (Metabolic Acidosis)

161
Q

Nursing interventions for Hypervolemia

A

I and O

weight

breath sounds

edema in the feet, ankles, and sacrum

lab value check (BUN and HCT)

Rest (favors diuresis)

response to diuretics

IV fluids

education on low sodium diet and self monitoring weight

upright position for dyspnea

turn and position

162
Q

Hyponatremia

A

Serum sodium level <135-145 mEq/L

d/t excessive sodium loss (without water) or excessive water gain (without sodium)

163
Q

The most common electrolyte imbalance in a hospital setting is ..

A

hyponatremia with a 3% prevalence

164
Q

Decreased Serum Osmolality in Hyponatremia leads to …

A

First fluid moves from the ECF to ICF to cause swelling, and the second shift then cocurs where sodium shifts from ICF to ECF

165
Q

Examples of electrolytes traveling together?

A

sodium and chloride

potassium, calcium, magnesium

166
Q

Most abundant lyte in the blood

A

Na+

167
Q

Most abundant lyte in the cell

A

K+

168
Q

Etiologies of Hyponatremia

A

Excessive Sodium Loss

Insufficient Sodium Intake or Absorption

Excessive Water Gain

Adrenal Insufficiency

SIADH

169
Q

Excessive Sodium Loss examples that cause Hyponatremia

A

prolonged diuretic therapy

burns

excessive diaphoresis

GI fluid loss: prolonged vomiting, NG suction, diarrhea, laxative abuse, repeated TWEs

renal disease

170
Q

Examples of things that lead to insufficient sodium intake or absorption leading to hyponatremia

A

anorexia

acute alcoholism

171
Q

Examples of things that lead to excessive water gain leading to hyponatremia

A

excessive administration of water PO or IV (D5W)

psychiatric disorders with compulsive water drinking

172
Q

How does adrenal insufficiency lead to hyponatremia?

A

low aldosterone compromises sodium reabsorption (and kidneys hold K instead)

173
Q

How does SIADH lead to hyponatremia?

A

dilutional hyponatremia d/t water retention

174
Q

Manifestations of Hyponatremia

A

Decreased Na+

I > O , decreased UO

decreased urine specific gravity (<1.010)

decreased Cl- (<100 mEq/L)

decreased serum osmolality (<285)

Weight gain - no significant edema

Fingerprinting over sternum

175
Q

What manifestations does decreased Na+ levels >125 lead to?

A

asymptomatic

176
Q

What manifestations does decreased Na+ levels 120-125

A

nausea
malaise
abd cramps

177
Q

What manifestations does decreased Na+ levels 115-120

A

headache
lethargy
obtunded

178
Q

What manifestations does decreased Na+ levels <110-115

A

seizures
coma
personality changes

179
Q

What is the hallmark of Hyponatremia?

A

Fingerprinting over the sternum

ONLY hyponatremia causes this

actual swelling of the cells, not in tissues or spaces, lead to this

180
Q

Cause and Effect of Hyponatremia

A

Causes: Excessive sodium loss or Sodium dilution with excess water

Effects: Increased water in the brain, headache, weakness, lethargy, confusion, GI issues like not wanting to eat and diarrhea, plasma sodium low and urine gravity is low

181
Q

A lot of issues occur ____ for hyponatremia

A

neurologically (d/t cell swelling)

182
Q

How to treat Hyponatremia

A

If its sodium loss: replace sodium PO or IV - NS for mild to moderate or 3% saline pump for severe (it is hypertonic so we dont wanna shift too fast from cells to circulatory system) (Na<120)

For excessive water gain - restrict fluid intake

183
Q

Nursing Interventions of Hyponatremia

A

Restrict Fluids (teach family, fluid restriction, post sign)

Accurate I and O (via IV pump)

Daily Weight

VS - BP and HR

Neurologic Assessment (LOC, pupillary responses, muscle strength)

Safety Precautions (side rails, seizures, precautions)

Monitor lab values

Turn and position

184
Q

The most important assessment for a hyponatremia patient is?

A

the Neurologic Assessment

185
Q

Hyponatremia has less salt in the blood, so where does fluid shift?

A

it will move into the cell which has higher salt concentration

186
Q

Hypernatremia

A

serum sodium level >145 mEq/L

d/t excessive sodium gain (without water) or excessive water loss (without sodium)

187
Q

What does the increased serum osmolality do for fluid shifting in hypernatremia?

A

fluid shifts from ICF to ECF (cellular shrinking)

There is a higher concentration in the blood so it must be diluted

188
Q

Hypernatremia is most often a ___ problem

A

water problem

never occurs in alert patients with normal thirst and access to water because of their thirst mechanism

189
Q

Etiologies for Hypernatremia

A

Water deprivation (i.e unconscious, debilitated, infants)

Hypertonic Tube Feedings (without water supplements)

Inadequately diluted baby formula

High protein diets (without adequate fluids)

Insensible water loss (i.e. burns hyperventilation or heat stroke)

Watery Diarrhea

Excessive administration of 3% saline (hypertonic) or sodium bicarb

Diabetes insipidus (lack ADH - water loss without salt loss)

Near drowning in sea water

190
Q

Manifestations of Hypernatremia

A

Dry Stick Mucous Membranes

Neurologic (CNS) issues like hyperactive DTRs, disorientation, agitation with stimulation, hallucinations, lethargy –> Coma

Neuromuscular issues like muscle twitching and convulsions

Extreme thirst

VS (increase T and HR, decreased BP)

Oliguria and Anuria

Lab values (increase Cl-, serum osmolality >295, urine specific gravity > 1.015)

191
Q

What are the hallmark symptoms of Hypernatremia?

A

Extreme Thirst

Dry Sticky Mucous Membranes

192
Q

Cause and effects of Hypernatremia

A

Causes: Excess salt intake, Decreased salt loss, lack off sufficient water intake

Effects: mucous membranes dry and sticky, intense thirst, tachycardia, agitation, restless - overall feelings hyper rather than lethargic

193
Q

Treatments for Hypernatremia

A

Slow correction
-with 1/2 NS or 1/4 NS (hypotonic solution) to get water into cells (but not too fast like with D5W so there is no fluid overload or brain swelling)

Drug Intervention
- ADH, DDAVP, Thiazide Diuretics

194
Q

What is the paradoxical effect of thiazide diuretics for hypernatremia and diabetes insipidus?

A

it causes keeping water but getting rid of sodium

195
Q

Hypernatremia Nursing Interventions

A

Identify Pts at Risk (i.e. hypertonic tube feeding or hypertonic TPN)

Monitor I&O, VS, Mental Status, Daily Weight, Assess mucous membranes, monitor lab values, ensure adequate fluid intake

teach about food salt contents, how to minimize salt intake, and salt restricted diets

196
Q

No less than how much salt should be given a day for renal patients and non-renal patients?

A

Renal - 1.5 g

Non-renal - 2000g

197
Q

Hypokalemia

A

Serum potassium levels (low) < 3.5 mEq/L

D/t excessive potassium excretion or inadequate potassium intake

198
Q

Normal K+ levels in a person?

A

3.5 to 5.5

199
Q

K is greatest in what area? And by how much?

A

It is the major cation in ICF inside cells, and is 28x greater in the cell than outside it

200
Q

Do we store excess K+?

A

no we get rid of excess with urine

201
Q

Etiologies for Hypokalemia

A

GI Losses (vomiting, diarrhea, suction, ileostomy, villous adenoma, alcoholism)

Intracellular shifts (metabolic alkalosis, DKA)

Anorexia Nervosa

Dialysis treatment (excess removal)

Excessive Insulin

Renal losses (d/t hyperaldosteronism, nephrotic syndrome, diuretics, drugs, excess steroid release [Cushing’s syndrome, excessive stress, tumors of adrenal cortex])

202
Q

K+ is essential for …

A

the heart and GI system function

203
Q

What typically regulates potassium?

A

The kidneys

204
Q

Why does Metabolic Alkalosis lead to Hypokalemia?

A

It is a decreased H+ concentration - to correct this H+ moves from the cell to the blood and K+ moves into the cell to correct alkalosis to maintain neutrality

If pH is above 7.45 this is metabolic alkalosis - low K+ in blood by correcting for H+ and moving into cells

205
Q

Manifestations of Hypokalemia

A

Decreased Serum Potassium

Cardiac issues (Dysrhythmias, digitalis toxicity)

Lab values (increased pH and bicarb, urine sg < 1.010, slight increase in serum glucose)

Muscular weakness

GI issues (anorexia, prolonged gastric emptying, gaseous distension, paralytic ileus)

Renal Issues (inability to concentrate urine - dilute urine, polyuria - nocturia, polydipsia)

206
Q

Digitalis Toxicity

A

it is a medicine and if there is not enough K+ it can be toxic for the heart

207
Q

How does muscular weakness progress in Hypokalemia?

A

it progresses from the extremities inward

208
Q

Cause and Effects of Hypokalemia

A

Causes: Decreased K intake, Increased Loss of K, Shift of K into cells

Effects: cardiovascular effects, kidney effects, muscle weakness

209
Q

Treatment for Hypokalemia

A

IV replacement (never give K in any form if there is no kidney function - there needs to be urine output before giving K) (never IV push K as it can lead to cardiac arrest) (mix thoroughly and it is an irritant)

Dietary (foods and salt substitutes)

Oral Supplements (administer w/ meals to decrease GI irritation, give with full glass of water, contraindicated if on K sparing diuretic)

210
Q

When is potassium oral supplements contraindicated?

A

When on a K Sparing Diuretic

Or with bad kidney function

211
Q

Why must you never pump more than 10 mEq/hr or in 100 mL over 1 hour with a pump for potassium?

A

It is IV pushing and can lead to arrythmias and potential cardiac arrest

212
Q

Hypokalemia Nursing Interventions

A

Prevention for Pts at risk

Monitor I and O

Cardiac Monitoring

Adminsiter Potassium Supplements

VS (HR, BP)

Monitor Lab Values (for alkalosis)

Teaching on dietary intake, salt supplements, and supplements to take with food

213
Q

What are some foods high in potassium

A

apricots

bananas

oranges

carrots

baked potatoes with skin

214
Q

How do you know kidney function is good enough for K treatment?

A

they have good urine output

215
Q

Hyperkalemia

A

Serum Potassium levels > 5.0 mEq/L

d/t excessive potassium intake or impaired potassium excretion

216
Q

Hyperkalemia seldom occurs in what situations?

A

In patients with normal kidney function

217
Q

What is the most common reason for Hyperkalemia?

A

Often due to iatrogenic causes and more common in hospitalized older adults

SO, its more common WHEN WE CAUSE IT

218
Q

What is more dangerous, hyperkalemia or hypokalemia

A

Hyperkalemia due to a higher risk for lethal arrhythmia (more likely to get dysrhythmia in hypokalemia)

219
Q

Etiologies for Hyperkalemia

A

Decreased Renal Excretion

Hypoaldosteronism (not holding enough Na and its leaving in urine and you have more K)

K Sparing Diuretics (block hypoaldosteronism)

Drugs (trimethoprim, NSAIDS, ACE inhibitors, B adrenergic drugs, cyclosporine)

Metabolic Acidosis

Tissue injury and lysis of cells (28x more in cells so release is bad)

Excessive oral or IV intake (use of potassium containing salt substitutes in RF)

Bowel obstruction

220
Q

Manifestations of Hyperkalemia

A

Cardiac Issues (high lethal arrhythmia issues; cardiac arrest; bradycardia)

CNS - confusion

Neuromuscular (muscle weakness, flaccidity, paresthesia, numbness, ascending paralysis from LEs)

GI (Nausea, intermittent colic, diarrhea)

Oliguria

221
Q

What EKG changes occur from Hyperkalemia?

A

Depressed ST Segment

Peaked T Waves

Widened QRS Complex

Prolonged PR Interval

Loss of P Waves

222
Q

What does ST Segment depression mean

A

ST segment does not return to isoelectric line - so ischemia occurs (hyperkalemia)

223
Q

What does Peaked T Waves mean

A

K sets the resting membrane potential so we get peaked T waves - which is abnormal (hyperkalemia)

224
Q

What does Widened QRS complex mean

A

signals have trouble going through the ventricle (hyperkalemia)

225
Q

What are the major manifestations of Hyperkalemia?

A

Cardiac Arrhythmias leading to cardiac arrest and bradycardia and CNS confusion

226
Q

How does metabolic acidosis lead to Hyperkalemia?

A

The body corrects acidosis (<7.35) by moving H+ into cells which moves K+ out into the blood

all comes from buffer system for pH

227
Q

What symptoms are in both hypo and hyperkalemia and therefore cannot tell you which it is alone?

A

Neuromuscular manifestations

228
Q

How does activity differ between Hyper and Hypokalemia?

A

Hyperactive - Hyperkalemia

Hypoactive - Hypokalemia

229
Q

Cause and Effect of Hyperkalemia

A

Cause: Excess intake, decreased loss, shift of K out of cells

Effects: Cardiac issues, muscle problems, GI vomiting/nausea, renal oliguria –> anuria, confusion

230
Q

Treatment for Hyperkalemia

A

Kayexalata PO or PR (Cation Exchange Resin)

IV Diuretics (if renal functioning properly)

Dialysis

231
Q

Kayexalate

A

cation exchange resin

must be used cautiously when person has HF must either take by mouth and excrete it in 24 hours with diarrheal stool or take a retention enema for 30-60 minutes with an indwelling cath

232
Q

Emergency Treatments for Hyperkalemia

A

Calcium Gluconate

Sodium Bicarbonate

GIK Mechanism (Insulin)

233
Q

Calcium Gluconate

A

slow IV infusion

protective mechanism for the heart - it increases the threshold to make sure the heart does not fire as quickly, but it does not get rid of potassium

234
Q

What is the mechanism of action for Calcium Gluconate

A

decreased K lowers resting membrane potential and increased K raises it

Ca++ raises the threshold to correct the difference from potassium

the difference is what usually causes arrhythmia

235
Q

How does sodium bicarbonate help treat Hyperkalemia?

A

it moves K into cells temporarily - could be life saving

236
Q

How does GIK treat Hyperkalemia?

A

Insulin moves BOTH K and Glc into cells - temporarily but a quick fix

Normal glc levels means give both insulin and glucose to remove K

237
Q

Nursing Interventions for Hyperkalemia?

A

Prevention for pts at risk

Monitor I and O

Cardiac Monitoring

Administer K depleting meds

VS watching (HR and BP)

Monitor lab values (acidosis)

Assess bowel function

Teach about renal failure and insufficiency, foods high in potassium, salt substitutes, and not using K sparing diuretics

Proper venipuncture technique (false potassium increases occur d/t cell lysis)

238
Q

Pseudohyperkalemia

A

false potassium increase from cell lysis from improper venipuncture technique

239
Q

EKG differences between Hypokalemia and Hyperkalemia

A

Hypo - flat T wave; Hyper - peak T wave

Both have depressed ST Segment

Hyper has prolonged PR interval potentially

240
Q

What is the EKG changes that signifies Hyperkalemia more so than others?

A

A peak T Wave

241
Q

What charge is Calcium ions

A

2+

242
Q

Hypocalcemia

A

Serum Calcium Level <8.5 mg/dL

d/t inadequate calcium intake or absorption, or excessive calcium excretion or elimination

243
Q

99% of Ca2_ is stored in ..

A

bones and teeth as calcium phosphate (so when it is released both phosphate and calcium release)

244
Q

Narrow calcium range in the blood ?

A

8.5 to 10.5 (since most is in bones or teeth)

245
Q

What happens with PTH when Ca2+ levels drop

A

PTH pulls from bones: so decreased Ca2+ causes increased PTH

246
Q

You can end up with weak brittle bones if there’s PTH too much because Parathyroid ___

A

pulls!

247
Q

What is needed to absorb calcium?

A

Vitamin D

248
Q

Why can loss of renal function lead to Hypocalcemia

A

we need the kidney to activate Vitamin D in order to absorb calcium

249
Q

How does Celiac disease influence Hypocalcemia?

A

it is a malabsorption problem that impacts the serum calcium levels

250
Q

How does calcium travel in the blood?

A

Calcium travels the blood freely in a metabolically active form that is ionized

50% of this is unbound calcium
50% is a form of calcium bound the plasma proteins

251
Q

___ calcium + ___ calcium = Total Serum Calcium Levels

A

Bound + Unbound = Total

252
Q

How does Total Calcium change and symptoms occur depending on how bound and unbound levels of calcium change?

A

If both levels lower, total calcium lowers

If plasma proteins are loss and there’s less bound calcium, but there is still unbound calcium present you also get lower total levels, BUT you will not get s/s if you have normal unbound ranges (ionized)

However, if things move from unbound to bound to correct imbalance, that wont be reflected in total Ca, so we do need to look at more to know Serum Calcium Levels

253
Q

What things may decreased bound calcium levels?

A

some with decreased protein intakes, nursing home residents, or liver disease get hypoalbuminemia and decreased plasma proteins –> decreased bound calcium with normal unbound still the same –> total calcium decrease but not S/S

254
Q

The body regulates via __ calcium

A

unbound calcium

bound is not metabolically active since its on proteins, only when unbound is high or low does hyper or hypocalcemia occur

255
Q

If protein or albumin levels are low you can infer what?

A

That bound calcium levels are low, especially is there is no s/s

256
Q

What form of calcium is more informative ?

A

Unbound/Ionized calcium

257
Q

S/S of Hypocalcemia and Hypercalcemia only occur when …

A

unbound calcium is low and total calcium lowers as a result

258
Q

A balance between what things allows for calcium homeostasis?

A

absorption from the gut, excretion from the kidney, and reabsorption or deposition from bone

259
Q

What cascade of actions fix low calcium levels?

A

Hypocalcemia –> PTH pulls calcium from bones, tells kidney to increase calcium reabsorption/activate Vitamin/excrete more PO4 3+, increases calcium uptake in GI tract

260
Q

What is the most important step of the bodies natural attempt to fix hypocalcemia?

A

Activation of Vitamin D, after the Kidneys get PTH, which leads to increased calcium uptake by GI

261
Q

Etiologies of Hypocalcemia

A

Post Op (Parathyroidectomy, thyroidectomy, radial neck dissection)

Renal Failure (d/t hyperphosphatemia)

Alkalosis (citrated blood)

Acute Pancreatitis

Drugs

Inadequate intake or absorption (anorexia, chrons, vit D deficiency, lack of sun exposure, etc)

Excessive elimination (low PTH levels d/t hypomagnesemia s/t alcoholism or diuretics)

Hypoalbuminemia

262
Q

Manifestations of Hypocalcemia

A

Neuromuscular (Calcium sets resting membrane potential so low amounts lead to firing sooners) - so muscular irritability, tingling, parathesias, cramps, spasms, tetany, seizure, positive chvostek and trousseau sign, hyperactive DTR.

CNS - confusion, anxiety, depression, psychosis, loss of sensorium

Cardiovascular - decreased Myocardial contractility, hypotension, dysrhythmia, EKG prolonged QT and ST

Hematologic - prolonged PT, PTT, bleeding and bruising (no calcium for the clotting cascade)

Overall irritability, hyperactivity, no clotting, low heart power, depressed CNS

263
Q

Trousseau’s Sign

A

Sign for Latent Tetany (spasm)

You pump 20 mmGHg above normal systolic, and if there is hypocalcemia leave it a minute and the patient will end up having a carpopedal spasm (arm twitch down)

It is a sign of neuromuscular irritability along with Chvostek’s sign

264
Q

Chvostek’s Sign

A

Sign for latent tetany (spasm)

Tap facial nerve, and the lip on that side of the face will twitch

It is a sign of neuromuscular irritability along with Trousseau’s Sign

265
Q

Cause and Effect of Hypocalcemia

A

Cause Decreased unbound calcium, inadequate intake, excess loss, decrease in GI tract and bone absorption

Effect: CNS issues, Cardiovascular system dysrhythmia (weak heart ability), increase GI tract irritability, abnormal calcium deposits, muscle tetany!

266
Q

Acute Hypocalcemia Treatment

A

Calcium gluconate via slow IV infusion

Need to monitor as calcium in the tissue can cause necrosis!

Do not give with Digoxin

The CaGlc cn prevent laryngospasm and protect the heart and life threatening spasm

267
Q

Chronic Hypocalcemia Treatment

A

Oral Calcium Supplements w/ Vit D an Mg

HRT - estrogen replacement, soy

Calcitonin (prevention in osteoporosis)

Fosamax (inhibits bone resorption)

268
Q

Whys is Fosamax a nasty drug?

A

must take upright

take firs tin the morning

must be taken on an empty stomach with water only

very nasty drug

269
Q

Nursing Interventions for Hypocalcemia

A

Prevention for pt at risk

Administer calcium supplements

calcium gluconate at bedside for thyroid/neck surgery

Cardiac monitoring

Maintain airway patency

Monitor lab values

Seizure/Safety Precautions (if severe)

teach about alcohol and cig influence, dietary sources, exercise (weight bearing exercise), estrogen

270
Q

Dietary Sources of Calcium

A

Dairy Products

Green Leafy Vegetables

271
Q

Hypercalcemia

A

Serum calcium levels > 10.5 mg dL

Acute > 13 mg/dL

Severe >16 mg/dL

d/t excessive calcium intake or absorption; or; increased release of calcium from bone

Occurs when the rate of calcium entry into the ECF . rate of renal calcium excretion

272
Q

Etiologies of Hypercalcemia

A

Excessive Intake of calcium supplements

Excessive use of calcium containing antacids

Excessive vitamin D intake (stims absorption)

Use of thiazide diuretics

Hyperparathyroidism (or tumor makes too much PTH pulling lots of calcium from bones)

Prolonged immobility

malignancies

drug

thyrotoxicosis

hypophosphatemia (means less exchange of calcium at kidney level)

milk alkali syndrome

273
Q

Milk alkali Syndrome

A

ingest sodium bicarbonate and get calcium from milk, they then combine to form extra calcium in the bloodstream

274
Q

Manifestations of Hypercalcemia

A

Neuromuscular (sedate effect, weakness, decreased DTRs)

GI (decreased motility, constipation(ca is chalky), anorexia, N/V)

CNS (confusion, memory impairment, bizarre behavior, decrease in LOC–> Coma) - decreased innervation leads to decreased nerve speed

Renal (polyuria, polydipsia, renal colic, renal failure from urinary calculi)

Cardiac (dysrhythmia, EKG shortened QT, increased BP)

Bone (soft tissue calcification, pathologic fractures)

275
Q

Why does polyuria and polydipsia occur with Hypercalcemia?

A

Glucose AND calcium increases tonicity of urine - so filtrate absorbs more fluid and polyuria occurs, with polydipsia since there is less fluid and you want to replace it

276
Q

Cause and Effect of Hypercalcemia

A

cause: loss from bones, excess intake, increase from factors increasing mobilization from bones

effect: cardiovascular system, bradycardia, dysrhythmia, kidney issues GI issues, muscle issues (EVERYTHING SLOWS DOWN MORE)

277
Q

Treatment for Hypercalcemia

A

High Fluid intake (3-4 L / day)

Eliminating contributing drugs (thiazides, vitamin D, calcium antacids)

Increase mobility

IV NS 200-500 mL/Hr to dilute calcium and increase GFR and loop diuretic prevents overload and increases excretion

Hourly I and O and breath sounds

Etidronate, Plicamycin, Calcitonin

278
Q

When is Etidronate (Didronel) used for Hypercalcemia

A

tx for malignancies that are NOT hyperparathyroidism

279
Q

When is Plicamycin (Mithracin) used for Hypercalcemia

A

tx for breath cancer

280
Q

How is Calcitonin used to treat Hypercalcitonin

A

skin test first

it decreases bone resorption by stopping PTH to protect bones and ionized calcium levels

temp effect of 6-10 days so you need to target the root cause still

281
Q

Nursing Interventions for Hypercalcemia

A

Prevention for Pts at risk

Increased mobility

Monitor I and O

3-4 L of fluid per day

Bulk fiber in diet to decrease constipation

Safety Precautions

Check for pathological fractures and digoxin toxicity

Encourage cranberry juice to increase calcium solubility in urine

Calcitonin

Monitor lab values

Teach about s/s to watch for and avoid dairy products and calcium containing antacids

282
Q

How is calcium balance regulated when calcium levels get high

A

Decreased PTH and Increased Calcitonin –> (d/t PTH) decreased renal activation of Vit D) –> DECREASED intestinal absorption of calcium, renal reabsorption of calcium and decreased excretion of phosphate, and calcium resorption from bone

283
Q

How is calcium balance regulated when calcium levels get lower

A

Increased PTH and Decreased Calcitonin –> (d/t PTH) Increased renal activation of Vit D –> INCREASED intestinal absorption of calcium, renal reabsorption of calcium and decreased excretion of phosphate, and calcium resorption from bone

284
Q

EKG differences between Hypocalcemia and Hypercalcemia ?

A

Hypo - prolonged ST segment and QT interval

Hyper - shortened ST segment and QT interval

285
Q

Second most abundant cation in the cell behind potassium?

A

Magnesium

286
Q

Percentages of Magnesium Cation distribution?

A

60% in bones

2% in ECF

38% in interstitial spaces

287
Q

Normal Magnesium levels

A

MG 1.5-2.3 mEq/L or 1.8 - 2.6 mg/dL

288
Q

Sources of magnesium

A

unprocessed cereal grains

nuts

chocolate

legumes

green leafy vegetables

dairy products

dried fruit

meat

fish

water not processed through a water softener

289
Q

Hypomagnesemia

A

A decreased serum Mg level of less than 1.5 mEq/L or 1.8 mg/dL

290
Q

Serum does not reflect ___!

A

Stores!

291
Q

Causes for hypomagnesemia

A

decreased Mg intake

excessive loss of calcium and potassium

vomiting

diarrhea

NG suction

GI losses

Intestinal malabsorption

Intestinal Fistulas

increased renal excretion

prolonged diuretic therapy

excessive aminoglycoside use

rapid administration of citrated blood

renal disease

chronic alcoholism

diabetic ketoacidosis

burns

pancreatitis

292
Q

Why does calcium and potassium loss lead to hypomagnesemia?

A

Magnesium moves with Potassium and Calcium together so loss of one leads to loss of the others

293
Q

Why does GI loss lead to hypomagnesemia so easily

A

There is a lot of Mg in the lower GI tract and intestinal absorption determines this so malabsorption here can lead to hypomagnesemia

294
Q

The biggest causes of hypomagnesemia are…

A

malabsorption

intestinal fistula

(things that impact GI tract (lower))

295
Q

Why does rapid citrated blood administration lead to hypomagnesemia

A

the preservative turns your blood alkalotic so buffer systems move things causing this

296
Q

What can be sued to treated hypomagnesemia from alcoholism

A

folate and multivitamins

297
Q

S/S of Hypomagnesemia

A

CNS - convulsions, paresthesia’s, tremor, ataxia

Mental changes - agitation, depression, confusion

Cardiovascular System- tachycardia, dysrhythmia

Muscle - cramps, spasticity, tetany, athetoid movement, BABINSKI REFLEX, CHVOSTEK SIGN

Neurologic irritability- tetany, weakness

EKG - broad T wae, ST shortened, Prolonged QT interval, and wide QRS complex - severe can invert T waves and prominent U waves

Laryngeal Stridor, coma, or sudden death if severe

298
Q

Why is babinski reflex abnormal in hypomagnsemia?

A

it usually is gone by an early age

299
Q

Implementation to care for Hypomagnesemia

A

Monitor VS, neuromuscular changes, I and Os

Initiate seizure precaution

Administer oral or IV magnesium

Monitor Ca2+ and K+ levels and administer both if levels are low as prescribed

Monitor for DTR suggesting hypermag when administering

Monitor serum Mg levels every 12-24 hours when client is receiving Mg by IV

Instruct client to eat food high in Mg Ca2+ and K+

300
Q

Hypermagnesemia

A

increased magnesium serum levels of 2.3 mEq/L or 2.6 mg/dL

301
Q

Causes of Hypermagnesemia

A

Advanced renal failure

excessive laxative use that contains magnesium

overuse of antacids (that have Mg)

ECF fluid deficit (concentrated with Mg)

Administration of Mg in toxemia of pregnancy

Untreated acute diabetic ketoacidosis

Hemodialysis w/ hard water or dialysate too high in Mg

Adrenal insufficiency

Pheochromocytoma (rare)

302
Q

Most common cause of Hypermagnesemia

A

Advanced Renal Failure

303
Q

S/S of Hypermagnesemia

A

Neurologic Depression - Slowing Down

Drowsiness

Lethargy

Bradycardia

Dysrhythmias

ECG shows peak T wave, prolonged PR and QT intervals, wide QRS

Respiratory Depression

Paralysis of resp center and voluntary muscles

severe hypotension along w/ nausea and vomiting

muscle weakness

areflexia

loss of DTR

coma

304
Q

Hypermagnesemia looks like ___ and ___

A

death and hypercalcemia

305
Q

Areflexia

A

no reflexes at all - dangerous

306
Q

Implementations for Hypermagnesemia Patients?

A

Monitor VS, Resp. Depression, hypotension, bradycardia, and dysrhythmias, neuro and muscular activity, LOC

remove source of excess Mg

increase renal excretion by forcing fluids or administering diuretics

administer 10% calcium gluconate as prescribed

mechanical ventilation in severe Mg excess

pacemaker for bradycardia

dialysis if renal function is impaired with Mg free dialysate

instruct clients regarding avoiding the use of laxatives and antacids containing Mg

307
Q

Calcium Glouconate protects the ___ and ___s Mg

A

protects the heart and antagonizes Mg

308
Q

EKG differences between Hypomagnesemia and Hypermagnesemia?

A

Hyper - wide QRS, prolonged PR, Tall T wave

Hypo - Prolonged QT, slightly longer PR, widened QRS, Flat T waves / broad flat T wave, prominent U wave

309
Q

What is in Hypomagnesemia’s unique EKG finding

A

Prominent U Wave

310
Q

Phosphorus Normal Values

A

3-4.5 mg/dL or 1.8-2.6 mEq/L

311
Q

What is a major anion in cells (negative charge)?

A

Phosphorus

312
Q

How is phosphorus distributed in the body?

A

85% of phosphorus in bones and teeth

less than 1% in blood

rest in soft tissue

313
Q

What is phosphorus responsible for

A

proper mineralization of bone and for energy metabolism - and is a part of ADP and ATP

314
Q

Sources of Phosphorus

A

Almonds
Dried Beans
Barley
Bran
Pumpkin
Squash
Cheese
Cocoa
Chocolate
Eggs
Lentils
Meats
Poultry
Pork
Beef
Legumes
Fish
Sardines
Liver
Milk
Oatmeal
Peanuts
Dried Peas
Walnuts
Wheat and Rye
Soft Drinks

315
Q

What kind of soft drink has more phosphorus?

A

darker color soft drinks - so renal patients that hold Phosphorus should not drink these

316
Q

Hypophosphatemia

A

serum phosphorus level below 3 mg/dL or below 1.8 mEq/L

below normal serum level

317
Q

Most phosphorus is absorbed in the ___ and excreted via the ___

A

phosphorus; kidneys

318
Q

Causes of Hypophosphatemia

A

Decreased Nutritional Intake

Poor Absorption from the bowel due to a lack of Vitamin D

Intake of carbonate antacids (may hinder absorption)

Malabsorption Syndrome

Increased renal excretion due to hyperparathyroidism or renal insufficiency

Diabetic Ketoacidosis

Steatorrhea

A poor nutritional state as in alcoholism

Fever

Long term TPN

Burns Hepatic Disease

319
Q

What is Phosphorus relationship to Calcium

A

they are inverse

so if you get rid of Calcium you keep Phosphorus and vice versa via level of kidneys

320
Q

Steatorrhea

A

fat in stools

floats

very smelly

321
Q

S/S in assessment of Hypophosphatemia

A

Anorexia
Dysphagia
Weakness
Malaise, Lethargy
Skeletal Pain and Aches
Bone Pain
Pathologic Fractures
Pulmonary Fractures
Tachypnea
Shallow Respiration
Confusion, Stupor, Delirium
Seizures
Hematologic Changes

Need Phosphorus for ATP so you have less energy!!!!
(A LOT OF THESE ARE SIMILAR TO HYPERCALCEMIA)

322
Q

If hypophosphatemia is occurring, what else is happening?

A

Hypercalcemia (so many s/s are similar)

323
Q

Implementations for Hypophosphatemia

A

Monitor respiratory status
Move client carefully
Administer potassium phosphate
Assess renal system before administering phosphorus
Monitor calcium, phosphorus, sodium, and chloride levels - renal failure DOES hold Phosphorus
Administer vitamin D
Monitor for decreased neuromuscular activity
Monitor for calcium excess and kidney stones
Monitor for hematologic changes
Monitor clients receiving TPN for electrolyte imbalances
Instruct client regarding the use of antacids

324
Q

When do kidney stones occur?

A

when calcium is exchanges and phosphorus leaves - so damage can occur

325
Q

Hyperphosphatemia

A

A serum phosphate level greater than 4.5 mg/dL or 2.6 mEq/L

Seen more clinically then hypophosphatemia

326
Q

Causes of Hyperphosphatemia

A

Excessive dietary intake of phosphorus

Overuse of phosphate containing laxatives or enemas

Hypoparathyroidism

Vitamin D intoxication (more vit D - more absorption)

Renal failure

Adrenal insufficiency

Excessive bone growth in infants and children (cows milk has more phosphorus than breast milk)

Metabolic and hormonal imbalances

Tissue damage

Parathyroid Surgery or Hypoparathyroidism

327
Q

S/S seen in Assessment for Hyperphosphatemia

A

Neurological Excitability

Hyperreflexia, tetany

Positive Chvostek’s or Trousseau’s Sign

Seizures

Conjunctivitis

Pruritis

Renal Deposits leading to renal failure

Opp of hypophosphatemia - looks like hypocalcemia

328
Q

Hyperphosphatemia goes alongside ___

A

hypocalcemia (since they exchange)

329
Q

What is seen more clinically, hyperphosphatemia and hypophosphatemia?

A

Hyperphosphatemia

330
Q

Pruritis

A

itching

331
Q

How does hyperphosphatemia instigate further renal failure?

A

Renal deposits occur from increased phosphorus that leads to deposits in renal tissue binding with calcium thus stimulating further renal failure

332
Q

Implementation of Nursing Interventions for Hyperphosphatemia

A

Increase fecal excretion of phosphorus by binding phosphorus from food in the GI tract (aluminum hydroxide gel)

Prepare for dialysis if prescribed

Administering calcium if hypocalcemia exists

Monitor neuromuscular irritability

Monitor for hyperreflexia, tetany, and seizures

Monitor for signs of hypocalcemia

Monitor for Trousseau’s and Chvostek’s signs

Instruct clients to avoid phosphate-containing
medications including laxatives and enemas

Instruct clients to decrease their intake of foods high in phosphorus

Instruct clients how to take phosphate-binding drugs emphasizing that they should be taken with meals or immediately after meals

N361: Pathophysiology II (20 decks)

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